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Hydrocodone / ibuprofen Disease Interactions

There are 26 disease interactions with hydrocodone / ibuprofen:

Major

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Impaired Gi Motility

Severe Potential Hazard, Moderate plausibility

Applies to: Inflammatory Bowel Disease, Constipation, Gastrointestinal Obstruction, Intestinal Anastomoses

Narcotic (opioid) analgesic agents increase smooth muscle tone in the gastrointestinal tract and decrease peristalsis, which can lead to elevated intraluminal pressure, spasm, and constipation following prolonged use. In patients with severe or acute inflammatory bowel disease, the decrease in colonic motility may induce toxic megacolon. Therapy with opioids should be administered cautiously in patients with gastrointestinal obstruction, constipation, inflammatory bowel disease, or recent gastrointestinal tract surgery. Gastrointestinal effects appear to be the most pronounced with morphine.

References

  1. White MJ, Berghausen EJ, Dumont SW, Tsueda K, Schroeder JA, Vogel RL, Heine MF, Huang KC "Side effects during continuous epidural infusion of morphine and fentanyl." Can J Anaesth 39 (1992): 576-82
  2. "Product Information. MS Contin (morphine)." Purdue Frederick Company, Norwalk, CT.
  3. "Product Information. Vicoprofen (hydrocodone-ibuprofen)." Knoll Pharmaceutical Company, Whippany, NJ.
View all 26 references
Major

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Infectious Diarrhea

Severe Potential Hazard, Moderate plausibility

Applies to: Infectious Diarrhea/Enterocolitis/Gastroenteritis

Narcotic (opioid) analgesic agents may prolong and/or worsen diarrhea associated with organisms that invade the intestinal mucosa, such as toxigenic E. coli, Salmonella, Shigella, and pseudomembranous colitis due to broad-spectrum antibiotics. These agents decrease gastrointestinal motility, which may delay the excretion of infective gastroenteric organisms and/or their toxins. Other symptoms and complications such as fever, shedding of organisms and extraintestinal illness may also be increased or prolonged. Therapy with opioids should be avoided or administered cautiously in patients with infectious diarrhea, particularly that due to pseudomembranous enterocolitis or enterotoxin-producing bacteria or if accompanied by high fever, pus, or blood in the stool.

References

  1. "Product Information. Darvon (propoxyphene)." Lilly, Eli and Company, Indianapolis, IN.
  2. "Product Information. Dalgan (dezocine)." Astra USA, Westborough, MA.
  3. "Product Information. Stadol (butorphanol nasal)." Bristol-Myers Squibb, Princeton, NJ.
View all 26 references
Major

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Liver Disease

Severe Potential Hazard, High plausibility

Applies to: Liver Disease

Narcotic (opioid) analgesic agents are extensively metabolized by the liver, and several of them (e.g., codeine, hydrocodone, meperidine, methadone, morphine, propoxyphene) have active metabolites that are further converted to inactive substances. The serum concentrations of these agents and their metabolites may be increased and the half-lives prolonged in patients with impaired hepatic function. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with liver disease. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

References

  1. "Product Information. Kadian (morphine)." Zeneca Pharmaceuticals, Wilmington, DE.
  2. "Product Information. Ultiva (remifentanil)." Glaxo Wellcome, Research Triangle Park, NC.
  3. "Product Information. Stadol (butorphanol)." Allscrips Pharmaceutical Company, Vernon Hills, IL.
View all 58 references
Major

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Prematurity

Severe Potential Hazard, High plausibility

Applies to: Prematurity/Underweight in Infancy

The use of narcotic (opioid) analgesic agents is contraindicated in premature infants. These agents may cross the immature blood-brain barrier to a greater extent than in adults, resulting in disproportionate respiratory depression.

References

  1. "Product Information. Calcidrine (codeine)." Abbott Pharmaceutical, Abbott Park, IL.
  2. "Multum Information Services, Inc. Expert Review Panel"
Major

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Renal Dysfunction

Severe Potential Hazard, High plausibility

Applies to: Renal Dysfunction

Although narcotic (opioid) analgesic agents are generally metabolized by the liver, renal impairment can alter the elimination of these agents and their metabolites (some of which are pharmacologically active), resulting in drug accumulation and increased risk of toxicity. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with significantly impaired renal function. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

References

  1. Wolff J, Bigler D, Christensen CB, et al "Influence of renal function on the elimination of morphine and morphine glucoronides." Eur J Clin Pharmacol 34 (1988): 353-7
  2. Chan K, Jennings F, Orme ML "Pharmacokinetics of low-dose intravenous pethidine in patients with renal dysfunction." J Clin Pharmacol 27 (1987): 516-22
  3. Aitkenhead AR, Vater M, Achola K, Cooper CM, Smith G "Pharmacokinetics of single-dose i.v. morphine in normal volunteers and patients with end-stage renal failure." Br J Anaesth 56 (1984): 813-9
View all 56 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Asthma

Severe Potential Hazard, High plausibility

Applies to: Asthma

Approximately 10% of patients with asthma may have aspirin-sensitive asthma, characterized by nasal polyposis, pansinusitis, eosinophilia, and precipitation of asthma and rhinitis attacks after ingestion of aspirin. The use of aspirin in these patients has been associated with severe bronchospasm and fatal anaphylactoid reactions. Since cross-sensitivity has been noted between aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs), therapy with any NSAID should be avoided in asthmatic patients with a history of aspirin or other NSAID sensitivity, and administered cautiously in all patients with preexisting asthma. Prior to initiating therapy with NSAIDs, patients should be questioned about previous allergic-type reactions to these agents. Salicylate salts, salsalate, salicylamide, and acetaminophen may be appropriate alternatives in patients with a history of NSAID-induced bronchospasm, since cross-sensitivity to these agents appears to be low. However, cross-sensitivity has been demonstrated occasionally with high dosages of these agents (e.g., acetaminophen >= 1000 mg), thus it may be appropriate to initiate therapy with low dosages and increase gradually. There is some evidence suggesting that COX-2 inhibitors may be safely used in patients with aspirin-sensitive asthma, although the labeling for these products contraindicate such use. If necessary, aspirin desensitization may also be attempted in some patients under medical surveillance.

References

  1. "Product Information. Voltaren (diclofenac)." Novartis Pharmaceuticals, East Hanover, NJ.
  2. "Product Information. Naprosyn (naproxen)." Syntex Laboratories Inc, Palo Alto, CA.
  3. Stevenson DD, Hougham AJ, Schrank PJ, Goldlust MB, Wilson RR "Salsalate cross-sensitivity in aspirin-sensitive patients with asthma." J Allergy Clin Immunol 86 (1990): 749-58
View all 38 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Fluid Retention

Severe Potential Hazard, Moderate plausibility

Applies to: Fluid Retention, Congestive Heart Failure, Hypertension

Fluid retention and edema have been reported in association with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). Therapy with NSAIDs should be administered cautiously in patients with preexisting fluid retention, hypertension, or a history of heart failure. Blood pressure and cardiovascular status should be monitored closely during the initiation of NSAID treatment and throughout the course of therapy.

References

  1. Heerdink ER, Leufkens HG, Herings RM, Ottervanger JP, Stricker BH, Bakker A "NSAIDs associated with increased risk of congestive heart failure in elderly patients taking diuretics." Arch Intern Med 158 (1998): 1108-12
  2. Lewis RV, Toner JM, Jackson PR, Ramsay LE "Effects of indomethacin and sulindac on blood pressure of hypertensive patients." Br Med J 292 (1986): 934-5
  3. "Product Information. Orudis (ketoprofen)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
View all 29 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Gi Toxicity

Severe Potential Hazard, High plausibility

Applies to: Peptic Ulcer, Gastrointestinal Hemorrhage, Gastrointestinal Perforation, Duodenitis/Gastritis, History - Peptic Ulcer, Alcoholism, Colitis/Enteritis (Noninfectious), Colonic Ulceration, Smoking

Nonsteroidal anti-inflammatory drugs (NSAIDs) can cause gastrointestinal mucosal damage, the risk of which appears to be related to both dosage and duration of therapy. Serious GI toxicity such as bleeding, ulceration and perforation can develop at any time, with or without warning symptoms, and occurs in approximately 1% of patients treated for 3 to 6 months and 2% to 4% of patients treated for one year. These trends continue with longer duration of use, although short-term therapy is not without risk. While agents that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) are generally thought to be associated with a reduced risk of GI toxicity compared to conventional NSAIDs, they have not been proven risk-free. In addition, there is evidence that COX-2 inhibitors may delay healing of gastric ulcers, and likely to the same extent as traditional NSAIDs. Thus, therapy with all NSAIDs, including COX-2 inhibitors, should be prescribed cautiously in patients with a history of peptic ulcer disease and/or gastrointestinal bleeding. Patients with such a history who use NSAIDs have a greater than 10-fold increased risk for developing a GI bleed compared to patients with neither of these risk factors. Caution is also advised if NSAIDs are prescribed to patients with other risk factors such as oral corticosteroid or anticoagulant use, alcohol use, smoking, older age, and poor general health status. Particular vigilance is necessary when treating elderly (i.e., age 60 years or more) and/or debilitated patients, since they are often more susceptible to the GI toxicity of these drugs and seem to tolerate ulceration and bleeding less well than younger, healthier individuals. Whenever possible, especially if prolonged use is anticipated, treatment with non-ulcerogenic agents should be attempted first. If NSAIDS are used, patients should be treated with the lowest effective dosage for the shortest duration possible, and prophylactic therapy with a cytoprotective agent (e.g., misoprostol), histamine H2-receptor antagonist, or a proton pump inhibitor should be administered as necessary. Patients should be counseled to avoid or minimize consumption of alcohol during NSAID therapy. Three or more alcoholic drinks per day during NSAID use may increase the risk of gastrointestinal ulceration and bleeding. Patients should also be advised to promptly seek medical attention if they experience symptoms that could indicate serious GI tract ulceration or bleeding such as epigastric pain, dyspepsia, melena, and hematemesis.

References

  1. Levy M, Miller DR, Kaufman DW, Siskind V, Schwingl P, Rosenberg L, Strom B, Shapiro S "Major upper gastrointestinal tract bleeding. Relation to the use of aspirin and other nonnarcotic analgesics." Arch Intern Med 148 (1988): 281-5
  2. Scott B "Bleeding massive gastric ulcer on diflunisal (Dolobid) ." Br Med J 1 (1979): 489
  3. "Product Information. Mobic (meloxicam)" Boehringer-Ingelheim, Ridgefield, CT.
View all 99 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Rash

Severe Potential Hazard, High plausibility

Applies to: Dermatitis - Drug-Induced

Severe, potentially fatal dermatologic reactions such as Stevens-Johnson syndrome, toxic epidermal necrolysis, and other exfoliative dermatitis have been associated with the use of nonsteroidal anti-inflammatory drugs (NSAIDs). These events may occur without warning. Patients should be advised to discontinue the NSAID and seek medical attention promptly at the first sign of rash, blisters, fever, itching, or any other sign of hypersensitivity.

References

  1. "Product Information. Indocin (indomethacin)." Merck & Co, Inc, West Point, PA.
  2. "Product Information. Tolectin (tolmetin)." McNeil Pharmaceutical, Raritan, NJ.
  3. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
View all 16 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Renal Toxicities

Severe Potential Hazard, High plausibility

Applies to: Renal Dysfunction, Dehydration, Congestive Heart Failure, Hyponatremia, Liver Disease

Chronic use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with renal toxicities, including elevations in serum creatinine and BUN, tubular necrosis, glomerulitis, renal papillary necrosis, acute interstitial nephritis, nephrotic syndrome, and renal failure. In patients with pre-renal conditions whose renal perfusion may be dependent on the function of prostaglandins, NSAIDs may precipitate overt renal decompensation via a dose-related inhibition of prostaglandin synthesis. Patients at greatest risk for this reaction include geriatric patients and those with impaired renal function, heart failure, liver dysfunction, or substantial volume and/or sodium depletion (e.g., due to diuretics). Therapy with NSAIDs should be administered cautiously in such patients, and hypovolemia and hyponatremia should be corrected prior to initiating treatment. Clinical monitoring of renal function is recommended during therapy, particularly in the presence of manifestations associated with mild azotemia (e.g., malaise, fatigue, loss of appetite). If renal function declines or renal failure occurs, prompt discontinuation of NSAID therapy will usually lead to recovery to the pretreatment state. NSAIDs are generally not recommended for patients with advanced renal disease due to the lack of information from controlled clinical studies regarding their use in such patients.

References

  1. Cefali EA, Poyner WJ, Sica D, Cox S "Pharmacokinetic comparison of flurbiprofen in end-stage renal disease subjects and subjects with normal renal function." J Clin Pharmacol 31 (1991): 808-14
  2. Shah GM, Muhalwas KK, Winer RL "Renal papillary necrosis due to ibuprofen." Arthritis Rheum 24 (1981): 1208-10
  3. Eriksson L-O, Sturfelt G, Thysell H, Wollheim FA "Effects of sulindac and naproxen on prostaglandin excretion in patients with impaired renal function and rheumatoid arthritis." Am J Med 89 (1990): 313-21
View all 152 references
Major

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Thrombosis

Severe Potential Hazard, High plausibility

Applies to: Cerebrovascular Insufficiency, History - Cerebrovascular Disease, History - Myocardial Infarction, Ischemic Heart Disease

The use of nonsteroidal anti-inflammatory drugs (NSAIDs) may be associated with an increased risk of cardiovascular thrombotic events such as myocardial infarction and stroke, which can be fatal. The risk may increase with duration of use. Clinical trials of several cyclooxygenase-2 (COX-2) selective and nonselective NSAIDs of up to three years duration have supported this association. Although not all NSAIDs have been studied, investigators believe it may be a class effect, and that the risk may be similar for all NSAIDs, both COX-2 selective and nonselective. Therapy with NSAIDs should be administered cautiously in patients with a history of cardiovascular or cerebrovascular disease. Patients should be treated with the lowest effective dosage for the shortest duration necessary. Appropriate antiplatelet therapy should be administered to patients requiring cardioprotection. However, there is no consistent evidence that concurrent use of aspirin mitigates the increased risk of serious cardiovascular thrombotic events associated with NSAID use, while the risk of serious GI events is increased. Patients should be advised to promptly seek medical attention if they experience symptoms that could indicate a cardiovascular thrombotic event such as chest pain, shortness of breath, weakness, and slurring of speech.

NSAIDs are contraindicated for the treatment of peri-operative pain in the setting of coronary artery bypass graft (CABG) surgery. Two large clinical trials of a COX-2 inhibitor for the treatment of pain in the first 10 to 14 days following CABG surgery found an increased incidence of myocardial infarction and stroke.

References

  1. "Product Information. Vioxx (rofecoxib)." Merck & Co, Inc, West Point, PA.
  2. Fitzgerald GA, Patrono C "The coxibs, selective inhibitors of cyclooxsygenase-2." N Engl J Med 345 (2001): 433-42
  3. Marcus AJ, Broekman MJ, Pinsky DJ "COX inhibitors and thromboregulation." N Engl J Med 347 (2002): 1025-6
View all 6 references
Major

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Acute Alcohol Intoxication

Severe Potential Hazard, High plausibility

Applies to: Alcoholism, Acute Alcohol Intoxication

The use of opiate agonists is contraindicated in patients with acute alcohol intoxication exhibiting depressed vital signs. The central nervous system depressant effects of opiate agonists may be additive with those of alcohol. Severe respiratory depression and death may occur. Therapy with opiate agonists should be administered cautiously in patients who might be prone to acute alcohol intake.

References

  1. "Product Information. Opium Tincture (opium)" Lilly, Eli and Company, Indianapolis, IN.
  2. "Product Information. MS Contin (morphine)." Purdue Frederick Company, Norwalk, CT.
  3. "Product Information. Vicoprofen (hydrocodone-ibuprofen)." Knoll Pharmaceutical Company, Whippany, NJ.
View all 15 references
Major

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Drug Dependence

Severe Potential Hazard, High plausibility

Applies to: Drug Abuse/Dependence, Alcoholism

Opiate agonists have the potential to cause dependence and abuse. Tolerance as well as physical and psychological dependence can develop after prolonged use. Abrupt cessation, reduction in dosage, or administration of an opiate antagonist such as naloxone may precipitate withdrawal symptoms. In patients who have developed tolerance to an opiate agonist, overdosage can still produce respiratory depression and death, and cross-tolerance usually will occur with other agents in the class. Addiction-prone individuals, such as those with a history of alcohol or substance abuse, should be under careful surveillance or medical supervision when treated with opiate agonists. It may be prudent to refrain from dispensing large quantities of medication to these patients. After prolonged use or if dependency is suspected, withdrawal of opiate therapy should be undertaken gradually using a dosage-tapering schedule.

References

  1. Fishbain DA, Goldberg M, Rosomoff RS, Rosomoff H "Atypical withdrawal syndrome (organic delusional syndrome) secondary to oxycodone detoxification ." J Clin Psychopharmacol 8 (1988): 441-2
  2. Strode SW "Propoxyphene dependence and withdrawal." Am Fam Physician 32 (1985): 105-8
  3. "Product Information. Levo-Dromoran (levorphanol)." Roche Laboratories, Nutley, NJ.
View all 26 references
Major

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Hypotension

Severe Potential Hazard, Moderate plausibility

Applies to: Dehydration, Hypotension, Shock

Opiate agonists can induce vasodilation and significant hypotension, particularly when given in high dosages and/or by rapid intravenous administration. Shock and cardiac arrest have occurred. At therapeutic analgesic dosages, ambulatory patients are more likely to experience dizziness and hypotension than patients who are confined to bed. However, orthostatic hypotension may occur in supine patients upon rising. Therapy with opiate agonists should be administered cautiously and initiated at reduced dosages in patients with circulatory shock, hypovolemia, or a predisposition to hypotension. When given by intramuscular or subcutaneous administration, clinicians should also be aware that impaired perfusion in these patients may prevent complete absorption of the drug. With repeated injections, an excessive amount may be absorbed suddenly if normal circulation is reestablished.

References

  1. Cox RG "Hypoxaemia and hypotension after intravenous codeine phosphate." Can J Anaesth 41 (1994): 1211-3
  2. "Product Information. OxyContin (oxycodone)." Purdue Frederick Company, Norwalk, CT.
  3. Sebel PS, Bovill JG, Boekhorst RA, Rog N "Cardiovascular effects of high-dose fentanyl anaesthesia." Acta Anaesthesiol Scand 26 (1982): 308-15
View all 23 references
Major

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Intracranial Pressure

Severe Potential Hazard, Moderate plausibility

Applies to: Brain/Intracranial Tumor, Head Injury, Cerebral Vascular Disorder

The hypoventilation associated with administration of opiate agonists, particularly by the intravenous route, can induce cerebral hypoxia and vasodilatation with resultant increase in intracranial pressure. Unless mechanical ventilation is provided, extreme caution is advised when opiate agonists are given to patients with head injury, intracranial lesions, or a preexisting elevated CSF pressure. Also, clinicians treating such patients should be aware that opiate agonists may interfere with the evaluation of CNS function, especially with respect to consciousness levels, respiratory status, and pupillary changes.

References

  1. "Product Information. Darvon (propoxyphene)." Lilly, Eli and Company, Indianapolis, IN.
  2. "Product Information. Fentanyl Oralet (fentanyl)." Abbott Pharmaceutical, Abbott Park, IL.
  3. "Product Information. OxyContin (oxycodone)." Purdue Frederick Company, Norwalk, CT.
View all 20 references
Major

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Respiratory Depression

Severe Potential Hazard, High plausibility

Applies to: Altered Consciousness, Asphyxia, Brain/Intracranial Tumor, Cerebral Vascular Disorder, Head Injury, Pulmonary Impairment, Sleep Apnea, Respiratory Arrest

Opiate agonists may produce significant central nervous system and respiratory depression of varying duration, particularly when given in high dosages and/or by rapid intravenous administration. Apnea may result from decreased respiratory drive as well as increased airway resistance, and rigidity of respiratory muscles may occur during rapid IV administration or when these agents are used in the induction of anesthesia. At therapeutic analgesic dosages, the respiratory effects are usually not clinically important except in patients with preexisting pulmonary impairment. Therapy with opiate agonists should be avoided or administered with extreme caution and initiated at reduced dosages in patients with severe CNS depression; sleep apnea; hypoxia, anoxia, or hypercapnia; upper airway obstruction; chronic pulmonary insufficiency; a limited ventilatory reserve; or other respiratory disorders. In the presence of excessive respiratory secretions, the use of opiate agonists may also be problematic because they decrease ciliary activity and reduce the cough reflex. Caution is also advised in patients who may be at increased risk for respiratory depression, such as comatose patients or those with head injury, intracranial lesions, or intracranial hypertension. Clinical monitoring of pulmonary function is recommended, and equipment for resuscitation should be immediately available if parenteral or neuraxial routes are used. Naloxone may be administered to reverse clinically significant respiratory depression, which may be prolonged depending on the opioid agent, cumulative dose, and route of administration.

References

  1. Redpath JB, Pleuvry BJ "Double-blind comparison of the respiratory and sedative effects of codeine phosphate and (+/-)-glaucine phosphate in human volunteers." Br J Clin Pharmacol 14 (1982): 555-8
  2. "Product Information. Dilaudid (hydromorphone)." Knoll Pharmaceutical Company, Whippany, NJ.
  3. "Product Information. Numorphan (oxymorphone)" Endo Laboratories LLC, Chadds Ford, PA.
View all 44 references
Moderate

Ibuprofen (Includes Hydrocodone/ibuprofen) ↔ Pku

Moderate Potential Hazard, High plausibility

Applies to: Phenylketonuria

Chewable products frequently may contain aspartame, which is metabolized in the gastrointestinal tract to phenylalanine. Motrin (brand of ibuprofen) chewable 50 mg and 100 mg tablets provide the equivalent of 3 mg and 6 mg of phenylalanine each, respectively. The aspartame/phenylalanine content should be considered when these and similar products are used in patients who must restrict their intake of phenylalanine (i.e. phenylketonurics).

References

  1. "Product Information. Motrin (ibuprofen)." Pharmacia and Upjohn, Kalamazoo, MI.
Moderate

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Adrenal Insufficiency

Moderate Potential Hazard, Moderate plausibility

Applies to: Adrenal Insufficiency

Patients with Addison's disease may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. Conversely, these agents may cause or potentiate adrenal insufficiency. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with adrenocortical insufficiency. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

References

  1. "Product Information. Orlaam (levomethadyl acetate)" Roxanne Laboratories Inc, Columbus, OH.
  2. "Product Information. Fentanyl Oralet (fentanyl)." Abbott Pharmaceutical, Abbott Park, IL.
  3. "Product Information. Roxanol (morphine)." Roxane Laboratories Inc, Columbus, OH.
View all 26 references
Moderate

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Biliary Spasm

Moderate Potential Hazard, Moderate plausibility

Applies to: Biliary Obstruction, Gallbladder Disease

Narcotic (opioid) analgesic agents increase smooth muscle tone in the biliary tract, which can lead to spasm and elevated biliary tract pressure, especially in the sphincter of Oddi. Biliary effects appear to be the most pronounced with morphine, although they do not always occur with therapeutic doses. Therapy with opioids should be administered cautiously in patients with biliary or gallbladder disease.

References

  1. "Product Information. Dalgan (dezocine)." Astra USA, Westborough, MA.
  2. "Product Information. Opium Tincture (opium)" Lilly, Eli and Company, Indianapolis, IN.
  3. "Product Information. MS Contin (morphine)." Purdue Frederick Company, Norwalk, CT.
View all 30 references
Moderate

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Hypothyroidism

Moderate Potential Hazard, Moderate plausibility

Applies to: Hypothyroidism, Panhypopituitarism

Patients with hypothyroidism may have increased risk of respiratory depression and prolonged CNS depression associated with the use of narcotic (opioid) analgesic agents. These agents may also exacerbate the effects of hypothyroidism such as lethargy, impaired mentation, depression, and constipation. Therapy with opioids should be administered cautiously and initiated at reduced dosages in patients with uncontrolled hypothyroidism or myxedema. Subsequent doses should be titrated based on individual response rather than a fixed dosing schedule.

References

  1. "Product Information. Numorphan (oxymorphone)" Endo Laboratories LLC, Chadds Ford, PA.
  2. "Product Information. Talwin NX (pentazocine)." Sanofi Winthrop Pharmaceuticals, New York, NY.
  3. "Product Information. Demerol (meperidine)." Sanofi Winthrop Pharmaceuticals, New York, NY.
View all 25 references
Moderate

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Seizure Disorders

Moderate Potential Hazard, Low plausibility

Applies to: Seizures

Narcotic (opioid) analgesic agents may exacerbate seizures in patients with seizure disorders and, at higher dosages, have been reported to induce seizures in patients without previous history of seizures. The proconvulsant activity may be the greatest with meperidine, the active metabolite of which is thought to be responsible. Therapy with opioids should be administered cautiously in patients with or predisposed to seizures.

References

  1. Strong WE, Matson M "Probable seizure after alfentanil." Anesth Analg 68 (1989): 692-3
  2. Armstrong PJ, Bersten A "Normeperidine toxicity." Anesth Analg 65 (1986): 536-8
  3. "Product Information. Dalgan (dezocine)." Astra USA, Westborough, MA.
View all 43 references
Moderate

Narcotic Analgesics (Includes Hydrocodone/ibuprofen) ↔ Urinary Retention

Moderate Potential Hazard, Moderate plausibility

Applies to: Urinary Retention

Narcotic (opioid) analgesic agents may inhibit the urinary voiding reflex and increase the tone of the vesical sphincter in the bladder. Acute urinary retention requiring catheterization may occur, particularly in patients with prostatic hypertrophy or urethral stricture and in elderly patients. These agents may also decrease urine production via direct effects on the kidney and central stimulation of the release of vasopressin. Therapy with opioids should be administered cautiously in patients with or predisposed to urinary retention and/or oliguria. The effects on smooth muscle tone appear to be the most pronounced with morphine.

References

  1. "Product Information. Calcidrine (codeine)." Abbott Pharmaceutical, Abbott Park, IL.
  2. "Product Information. Talwin NX (pentazocine)." Sanofi Winthrop Pharmaceuticals, New York, NY.
  3. "Product Information. Demerol (meperidine)." Sanofi Winthrop Pharmaceuticals, New York, NY.
View all 29 references
Moderate

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Anemia

Moderate Potential Hazard, Moderate plausibility

Applies to: Anemia, Bleeding

Dose-dependent decreases in serum hemoglobin and hematocrit have been observed in patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). Anemia has been reported occasionally. The mechanism may involve NSAID-induced fluid retention or gastrointestinal blood loss, or an incompletely described effect on erythropoiesis. The decreases in hemoglobin concentration tend to be slight with average doses but may exceed 1 g/dL when large doses are given, such as those used to treat osteoarthritis or rheumatoid arthritis. Although these effects are generally not clinically important in otherwise healthy individuals, they may be relevant in patients with preexisting anemia or substantial blood loss. Therapy with NSAIDs should be administered cautiously in patients with or predisposed to anemia. Clinical monitoring of hematopoietic function may be appropriate, particularly during chronic therapy.

References

  1. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
  2. Salom IL, Jacob G, Jallad N, Perdomo CA, Mullane JF, Weidler D "Gastrointestinal microbleeding associated with the use of etodolac, ibuprofen, indomethacin, and naproxen in normal males." J Clin Pharmacol 24 (1984): 240-6
  3. Squires JE, Mintz PD, Clark S "Tolmetin-induced hemolysis." Transfusion 25 (1985): 410-3
View all 49 references
Moderate

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Hepatotoxicity

Moderate Potential Hazard, Moderate plausibility

Applies to: Liver Disease

Borderline elevations of serum transaminases, LDH, and alkaline phosphatase have been reported in up to 15% of patients treated with nonsteroidal anti-inflammatory drugs (NSAIDs). These abnormalities may progress, remain unchanged, or regress with continuing therapy. Notable liver enzyme elevations exceeding 3 times the upper limit of normal have been reported in approximately 1% of patients in clinical trials. In addition, rare cases of severe hepatotoxicity, including liver necrosis, hepatic failure, jaundice and fatal fulminant hepatitis, have been reported. Therapy with NSAIDs should be administered cautiously in patients with preexisting liver disease. Periodic monitoring of liver function is recommended during prolonged therapy. NSAIDs are also highly protein-bound and some are extensively metabolized by the liver. Metabolic activity and/or plasma protein binding may be altered in patients with hepatic impairment. A dosage reduction may be required in some cases.

References

  1. "Product Information. Orudis (ketoprofen)." Wyeth-Ayerst Laboratories, Philadelphia, PA.
  2. Mroszczak EJ, Lee FW, Combs D, Sarnquist FH, Huang BL, Wu AT, Tokes LG, Maddox ML, Cho DK "Ketorolac tromethamine absorption, distribution, metabolism, excretion, and pharmacokinetics in animals and humans." Drug Metab Dispos 15 (1987): 618-26
  3. Dhand AK, LaBrecque DR, Metzger J "Sulindac (clinoril) hepatitis." Gastroenterology 80 (1981): 585-6
View all 92 references
Moderate

Nsaids (Includes Hydrocodone/ibuprofen) ↔ Platelet Aggregation Inhibition

Moderate Potential Hazard, Moderate plausibility

Applies to: Thrombocytopathy, Coagulation Defect, Thrombocytopenia, Bleeding, Vitamin K Deficiency

Nonsteroidal anti-inflammatory drugs (NSAIDs) reversibly inhibit platelet adhesion and aggregation and may prolong bleeding time in some patients. With the exception of aspirin, the platelet effects seen with most NSAIDs at usual recommended dosages are generally slight and of relatively short duration but may be more pronounced in patients with underlying hemostatic abnormalities. Thrombocytopenia has also been reported rarely during NSAID use. Therapy with NSAIDs should be administered cautiously in patients with significant active bleeding or a hemorrhagic diathesis, including hemostatic and/or coagulation defects associated with hemophilia, vitamin K deficiency, hypoprothrombinemia, thrombocytopenia, thrombocytopathy, or severe hepatic impairment. NSAIDs that selectively inhibit cyclooxygenase-2 (i.e., COX-2 inhibitors) do not appear to affect platelet function or bleeding time at indicated dosages and may be preferable if risk of bleeding is a concern.

References

  1. "Product Information. Relafen (nabumetone)." SmithKline Beecham, Philadelphia, PA.
  2. Leese PT, Hubbard RC, Karim A, Isakson PC, Yu SS, Geis GS "Effects of celecoxib, a novel cyclooxygenase-2 inhibitor, on platelet function in healthy adults: A randomized, controlled trial." J Clin Pharmacol 40 (2000): 124-32
  3. Hyson CP, Kazakoff MA "A severe multisystem reaction to sulindac." Arch Intern Med 151 (1991): 387-8
View all 56 references
Moderate

Opiate Agonists (Includes Hydrocodone/ibuprofen) ↔ Arrhythmias

Moderate Potential Hazard, Low plausibility

Applies to: Arrhythmias

Opiate agonists have cholinergic activity. Large doses and/or rapid intravenous administration may produce bradycardia and arrhythmia via stimulation of medullary vagal nuclei. Unlike other agents in the class, meperidine also has anticholinergic activity and may cause either bradycardia or tachycardia. Therapy with opiate agonists should be administered cautiously in patients with a history of arrhythmias. Clinical monitoring of cardiovascular status is recommended during therapy. Bradycardia and other cholinergic effects produced by these agents may be controlled with atropine.

References

  1. "Product Information. Opium Tincture (opium)" Lilly, Eli and Company, Indianapolis, IN.
  2. "Product Information. Duragesic Transdermal System (fentanyl)." Janssen Pharmaceutica, Titusville, NJ.
  3. "Product Information. Alfenta (alfentanil)." Janssen Pharmaceutica, Titusville, NJ.
View all 21 references

hydrocodone / ibuprofen drug Interactions

There are 1007 drug interactions with hydrocodone / ibuprofen

hydrocodone / ibuprofen alcohol/food Interactions

There are 2 alcohol/food interactions with hydrocodone / ibuprofen

Drug Interaction Classification

The classifications below are a general guideline only. It is difficult to determine the relevance of a particular drug interaction to any individual given the large number of variables.

Major Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.
Moderate Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.
Minor Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.

Do not stop taking any medications without consulting your healthcare provider.

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